25 research outputs found

    Fifteen years of the Australian imaging, biomarkers and lifestyle (AIBL) study: Progress and observations from 2,359 older adults spanning the spectrum from cognitive normality to Alzheimer\u27s disease

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    Background: The Australian Imaging, Biomarkers and Lifestyle (AIBL) Study commenced in 2006 as a prospective study of 1,112 individuals (768 cognitively normal (CN), 133 with mild cognitive impairment (MCI), and 211 with Alzheimer\u27s disease dementia (AD)) as an \u27Inception cohort\u27 who underwent detailed ssessments every 18 months. Over the past decade, an additional 1247 subjects have been added as an \u27Enrichment cohort\u27 (as of 10 April 2019). Objective: Here we provide an overview of these Inception and Enrichment cohorts of more than 8,500 person-years of investigation. Methods: Participants underwent reassessment every 18 months including comprehensive cognitive testing, neuroimaging (magnetic resonance imaging, MRI; positron emission tomography, PET), biofluid biomarkers and lifestyle evaluations. Results: AIBL has made major contributions to the understanding of the natural history of AD, with cognitive and biological definitions of its three major stages: preclinical, prodromal and clinical. Early deployment of Aβ-amyloid and tau molecular PET imaging and the development of more sensitive and specific blood tests have facilitated the assessment of genetic and environmental factors which affect age at onset and rates of progression. Conclusion: This fifteen-year study provides a large database of highly characterized individuals with longitudinal cognitive, imaging and lifestyle data and biofluid collections, to aid in the development of interventions to delay onset, prevent or treat AD. Harmonization with similar large longitudinal cohort studies is underway to further these aims

    Down from the treetops: Red langur (Presbytis rubicunda) terrestrial behaviour

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    Using direct observations and camera traps at eight sites across Indonesian Borneo we show how red langurs (Presbytis rubicunda) are more terrestrial than previously believed, regularly coming to the ground. This unusual behavior has been found at six of the eight sites surveyed. We find that red langurs come to the ground more frequently in disturbed forests, specifically ones which have been impacted by logging, fire, and hunting, though more data are needed to confirm this as a direct correlation. We also found a trend towards decreased ground use with increased elevation of the habitat. When on the ground, red langurs are predominantly engaged in feeding (50% direct observations, 61% camera traps) and traveling (29% direct observations, 13% camera traps). Red langurs are found on the ground throughout the day, at similar times to activity periods of the apex predator, the Sunda clouded leopard (Neofelis diardi). We suggest that ground use by red langurs could be an adaptation to disturbed forest to exploit additional food sources and to facilitate travel

    Cigarette smokers have exaggerated alveolar barrier disruption in response to lipopolysaccharide inhalation

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    RATIONALE: Cigarette smoke exposure is associated with an increased risk of the acute respiratory distress syndrome (ARDS); however, the mechanisms underlying this relationship remain largely unknown. OBJECTIVE: To assess pathways of lung injury and inflammation in smokers and nonsmokers with and without lipopolysaccharide (LPS) inhalation using established biomarkers. METHODS: We measured plasma and bronchoalveolar lavage (BAL) biomarkers of inflammation and lung injury in smokers and non-smokers in 2 distinct cohorts of healthy volunteers, one unstimulated (n=20) and one undergoing 50 µg LPS inhalation (n=30). MEASUREMENTS AND MAIN RESULTS: After LPS inhalation, cigarette smokers had increased alveolar capillary membrane permeability as measured by BAL total protein, compared to nonsmokers (median: 274 vs 208 µg/mL, p = 0.04). Smokers had exaggerated inflammation compared to nonsmokers, with increased BAL interleukin-1β (p = 0.002), neutrophils (p = 0.02), plasma interleukin-8 (p = 0.003), and plasma matrix metalloproteinase-8 (p = 0.006). Alveolar epithelial injury after LPS was more severe in smokers than non-smokers, with increased plasma (p = 0.04) and decreased BAL (p = 0.02) surfactant protein D. Finally, smokers had decreased BAL vascular endothelial growth factor (VEGF) (p < 0.0001) with increased soluble VEGF receptor-1 (p = 0.0001). CONCLUSIONS: Cigarette smoke exposure may predispose to ARDS through an abnormal response to a “second hit,” with increased alveolar-capillary membrane permeability, exaggerated inflammation, increased epithelial injury and endothelial dysfunction. LPS inhalation may serve as a useful experimental model for evaluation of the acute pulmonary effects of existing and new tobacco products
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